粒粒橙饮料的分层与汁胞萎瘪褪色的初步研究

本文研究了热因子对琼脂悬浮稳定性的影响,分析了造成汁胞萎瘪褪色的原因,并提出了解决的办法。认为只要琼脂的加热时间不要太长,分层现象是比较容易解决的。海藻酸钙凝胶薄膜和含油溶剂预处理能很好地防止汁胞的萎瘪破碎,但操作不当容易造成褪色。     

Knockout of SlNPR1 enhances tomato plants resistance against Botrytis cinerea by modulating ROS homeostasis and JA/ET signaling pathways

Tomato is one of the most popular horticultural crops, and many commercial tomato cultivars are particularly susceptible to Botrytis cinerea. Non-expressor of pathogenesis-related gene 1 (NPR1) is a critical component of the plant defense mechanisms. However, our understanding of how SlNPR1 influences disease resistance in tomato is still limited. In this study, two independent slnpr1 mutants were used to study the role of SlNPR1 in tomato resistance against B. cinerea. Compared to (WT), slnpr1 leaves exhibited enhanced resistance against B. cinerea with smaller lesion sizes, higher activities of chitinase (CHI), β-1, 3-glucanases (GLU) and phenylalanine ammonia-lyase (PAL), and significantly increased expressions of pathogenesis-related genes (PRs). The increased activities of peroxidase (POD), ascorbate peroxidase (APX) and decreased catalase (CAT) activities collectively regulated reactive oxygen species (ROS) homeostasis in slnpr1 mutants. The integrity of the cell wall in slnpr1 mutants was maintained. Moreover, the enhanced resistance was further reflected by induction of defense genes involved in jasmonic acid (JA) and ethylene (ET) signaling pathways. Taken together, these findings revealed that knocking out SlNPR1 resulted in increased activities of defense enzymes, changes in ROS homeostasis and integrity of cell walls, and activation of JA and ET pathways, which confers resistance against B. cinerea in tomato plants.     

Ceramide Production Mediates Aldosterone-Induced Human Umbilical Vein Endothelial Cell (HUVEC) Damages

Here, we studied the underlying mechanism of aldosterone (Aldo)-induced vascular endothelial cell damages by focusing on ceramide. We confirmed that Aldo (at nmol/L) inhibited human umbilical vein endothelial cells (HUVEC) survival, and induced considerable cell apoptosis. We propose that ceramide (mainly C18) production might be responsible for Aldo-mediated damages in HUVECs. Sphingosine-1-phosphate (S1P), an anti-ceramide lipid, attenuated Aldo-induced ceramide production and following HUVEC damages. On the other hand, the glucosylceramide synthase (GCS) inhibitor PDMP or the ceramide (C6) potentiated Aldo-induced HUVEC apoptosis. Eplerenone, a mineralocorticoid receptor (MR) antagonist, almost completely blocked Aldo-induced C18 ceramide production and HUVEC damages. Molecularly, ceramide synthase 1 (CerS-1) is required for C18 ceramide production by Aldo. Knockdown of CerS-1 by targeted-shRNA inhibited Aldo-induced C18 ceramide production, and protected HUVECs from Aldo. Reversely, CerS-1 overexpression facilitated Aldo-induced C18 ceramide production, and potentiated HUVEC damages. Together, these results suggest that C18 ceramide production mediates Aldo-mediated HUVEC damages. MR and CerS-1 could be the two signaling molecule regulating C18 ceramide production by Aldo.     

鲑鱼生长激素基因分泌型表达质粒的构建

生长激素(GH)是动物垂体前叶分泌的一种多肽类激素.应用分子重组及PCR等技术,构建了一种鲑鱼生长激素基因分泌型表达质粒pOsGH153,使编码鲑鱼生长激素成熟肽的序列克隆在大肠杆菌分泌型表达载体PIN-Ⅲ-ompA内,直接位于编码大肠杆菌外膜蛋白A信号肽序列的下游,在Lpp-Lac杂合启动子控制下,经IPTG诱导,分子量约23 000的鲑鱼生长激素在大肠杆菌中获得高效表达,该产物具有天然鲑鱼生长激素的免疫活性,直接分泌到细胞周质,而信号肽被自动剪除.     

Association between variants of EXT2 and type 2 diabetes: a replication and meta-analysis

Recent publications have found an association between variants of exostosin 2 (EXT2) gene and the risk of type 2 diabetes in some population but not in others. In an attempt to address these inconsistencies, we investigated EXT2 variants in two independent cohorts, and conducted a literature-based meta-analysis. Through regression model, we assessed the relationship between the EXT2 single nucleotide polymorphisms (SNPs) (rs3740878, rs11037909 and rs1113132) and the risk of type 2 diabetes in Han Chinese population, including a total of 2,533 cases and 2,643 controls. We combined our data with that from previously published studies and performed a meta-analysis to evaluate the effect size of the gene. Consistent with some studies, we found marginal association for the rs3740878 (OR = 1.07, 95 % CI = 0.99, 1.16, p = 0.09), rs11037909 (OR = 1.07, 95 % CI = 0.99, 1.16, p = 0.08), and rs1113132 (OR = 1.08, 95 % CI = 1.00, 1.17, p = 0.06) in our 2 cohorts. Meta-analysis, comprising 9,224 type 2 diabetes and 10,484 controls, revealed that three SNPs (rs3740878, rs11037909 and rs1113132) in EXT2 were significantly associated with type 2 diabetes (ORs range from 1.06 to 1.07, p = 0.038, p = 0.008 and p = 0.005, respectively). Variation in the EXT2 locus appears to be associated with a small increase in the risk of type 2 diabetes. However, well-designed prospective studies with larger sample size and more ethnic groups are needed to further validate the results.     

CREB up-regulates long non-coding RNA,HULC expression through interaction with microRNA-372 in liver cancer

Long non-coding RNA (lncRNA), highly up-regulated in liver cancer (HULC) plays an important role in tumorigenesis. Depletion of HULC resulted in a significant deregulation of several genes involved in liver cancer. Although up-regulation of HULC expression in hepatocellular carcinoma has been reported, the molecular mechanisms remain unknown. In this study, we used in vivo and in vitro approaches to characterize cancer-dependent alterations in the chromatin organization and find a CREB binding site (encompassing from −67 to −53 nt) in the core promoter. Besides, we also provided evidence that PKA pathway may involved in up-regulation of HULC. Furthermore, we demonstrated HULC may act as an endogenous ‘sponge’, which down-regulates a series of microRNAs (miRNAs) activities, including miR-372. Inhibition of miR-372 leads to reducing translational repression of its target gene, PRKACB, which in turn induces phosphorylation of CREB. Over-expression of miR-372 decreases the association of CREB with the proximal promoter, followed by the dissociation of P300, resulting in a change of the histone ‘code’, such as in deacetylation and methylation. The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it’s inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer.     

缺氧条件下冻伤对大鼠微循环血液灌流量的影响

本文采用体重２００±２０ｇ健康雄性Ｗｉｓｔａｒ大鼠,随机分为平原冻伤（ＦＮ）组、急性缺氧冻伤（ＦＡＨ）组和缺氧习服缺氧冻伤（ＦＨＡＣ）组,实验观察了大鼠右后肢重度冻伤前后各组大鼠双后肢皮肤微循环灌流量的改变。结果表明,平原冻伤使大鼠双后肢微循环灌流量明显减少,提示局部重度冻伤对微循环的影响不只局限于冻区也涉及到对侧肢体。冷冻前ＦＡＨ组大鼠微循环灌流量已明显低于ＦＮ组,表明急性缺氧时血容量进行代偿性的再分配,使微循环灌流量减少;ＦＡＨ组大鼠冻后双后肢微循环灌流量的改变结果提示急性缺氧可加重其冻伤对微循环的损伤程度。ＦＨＡＣ组大鼠冻前微循环灌流量非常明显地低于正常对照,也明显低于急性缺氧对照,表明缺氧习服可造成微循环障碍;ＦＨＡＣ组大鼠冻肢微循环灌流量非常明显地低于ＦＮ组,提示缺氧习服加重高原冻伤引起的微循环障碍。